pancreatic necrosis: paradigm of a multidisciplinary team

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Page 1: Pancreatic Necrosis: Paradigm of a Multidisciplinary Team

Advances in Surgery 40 (2006) 107–118

ADVANCES IN SURGERY

Pancreatic Necrosis: Paradigmof a Multidisciplinary Team

Mehran Fotoohi, MDa, L. William Traverso, MDb,*aDepartment of Radiology, Virginia Mason Medical Center,1100 Ninth Avenue, PO Box 900 (C6-GSURG), Seattle, WA 98111, USAbDepartment of General Surgery, Virginia Mason Medical Center,1100 Ninth Avenue, PO Box 900 (C6-SURG), Seattle, WA 98111, USA

Any discussion of pancreatic necrosis requires a set of acceptable and firmdefinitions. The reader should seek a comfort zone with the definitionsof necrosis, nonenhancement, parenchymal versus peripancreatic ne-

crosis, and sterile versus infected necrosis. To begin this discussion we shouldfirst give credit to the work of Edward L. Bradley III, who spearheaded a clin-ically ased classification system for acute pancreatitis, also known as the AtlantaCriteria [1]. In this document, six levels of acute pancreatitis are defined, from‘‘mild acute pancreatitis’’ to ‘‘pancreatic necrosis.’’ The definition of pancreaticnecrosis is ‘‘a diffuse or focal area(s) of nonviable pancreatic parenchyma,which is typically associated with peri-pancreatic fat necrosis.’’ The definitionof ‘‘nonviable pancreatic parenchyma’’ for clinical criteria is based on dynamiccontrast-enhanced CT scans showing nonenhancement. One also must under-stand the quantitative measure for nonenhancement.

Nonenhancement means the contrast density is <50 Hounsfield units, and bythe Atlanta definition of necrosis, there must be >3 cm of nonenhancement (or>30% of the area of the gland involved, either focally or diffusely). Because thepancreatic enhancement is commonly obscured by peripancreatic fat necrosis,the estimation of the extent of necrosis becomes unreliable and ‘‘semi-quantita-tive.’’ The accuracy of CT to demonstrate pancreatic parenchymal necrosis isbelieved to be more than 90%, yet an estimate of nonenhancement is still some-what subjective. The reader should assess the literature with caution for severalreasons. The quantitative assessment for nonenhancement is based on older CTtechnology; the extent of nonenhancement may be distorted by vasoconstrictionor inflammation and peripancreatic necrosis, and the radiologist assessment attimes can be subjective. CT technology for quantifying necrosis is not infallible.

A note here also must address how necrosis is determined to be present andthe location of necrosis (ie, parenchymal, peripancreatic, or both). Each pub-lished report should be scrutinized because studies may use a clinical definition

*Corresponding author. E-mail address: [email protected] (L.W. Traverso).

0065-3411/06/$ – see front matterª 2006 Elsevier Inc. All rights reserved.doi:10.1016/j.yasu.2006.05.007

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rather than a pathologic one. The latter is more reliable, because macroscopi-cally there is no question if the tissue is necrotic at surgery or autopsy. Thereader must remember that pancreatic parenchymal necrosis that is observedby CT rarely involves the entire gland and fat necrosis may be totally peri-pancreatic with only a focal area of pancreatic parenchymal necrosis (as is dis-cussed in this article).

Another controversy involves the clinical distinction of sterile versus infectedpancreatic necrosis. The mortality rate generally is believed to be much higherwith infected necrosis. The literature has pursued the concept that fine-needleaspiration of necrosis that does not yield bacteria most likely establishes a diag-nosis of ‘‘sterile pancreatic necrosis.’’ Generally it is also believed that sterilenecrosis can be treated without surgical intervention. This view also impliesthat any infected necrosis is fatal without surgical drainage. Our conceptfrom the paradigm that follows is that all patients believed to have ‘‘pancreaticnecrosis,’’ whether sterile or infected, should have future treatment decided bytheir clinical course based on clinical judgment and not on tests. We also wouldlike to update our readers on the idea that any patient with a deteriorating clin-ical course, whether infected or not, should undergo a trial of percutaneousdrainage. We have shown that most patients can avoid surgery, whether in-fected or not infected, with this multidisciplinary approach to pancreatic necro-sis [2]. The authors emphasize the word ‘‘multidisciplinary,’’ for without adedicated always available team, our algorithm should not be used.

OBJECTIVEPancreatic necrosis implies a permanent condition that results when a portion ofthe pancreas loses its blood supply. This condition is irreversible, yet many casesof necrosis culminate in a patient with a normal pancreas by CT or EndoscopicRetrograde Cholangiopancreatography (ERCP) after the patient recovers. Theconfusion is in an overreliance on imaging and in our less-than-firm definitions.The reader must be comfortable with simple definitions for the following keyitems: pancreatic ductal disruption, peripancreatic fluid collections, pseudocyst,pancreatic abscess, and pancreatic necrosis. Once known, the reader should real-ize that surgery alone is not enough. In the new millennium an array of disciplinesis required to lower the need for necrosectomy and achieve single-digit mortality.A multidisciplinary team with multiple areas of expertise and techniques canachieve the low values for the need for necrosectomy and mortality (Fig. 1).

DEFINITIONSTo be redundant, pancreatic necrosis implies a permanent condition that oc-curs when a portion of the pancreas loses its blood supply. It is irreversible,yet many cases of necrosis culminate in a patient with a normal pancreas onCT and ERCP. The confusion resides in correct interpretation of imaging stud-ies and then having a reasonable definition of the phases of severe pancreatitis,only one of which is necrosis.

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Mild to severe complications of necrosis ensue, depending on the extent ofnecrosis. Almost every severe case of pancreatitis is associated with a pancreaticduct disruption with or without necrosis. Unclear is which of the events oc-curred first—necrosis or ductal disruption. We believe that almost every caseof severe pancreatitis is made worse by a plumbing problem in the form ofa leak. The presence of a ductal disruption is significantly associated with thepresence of necrosis, higher mortality, and increased length of stay in the hos-pital [3]. Pancreatic necrosis and pancreatic ductal disruptions are integrally en-twined. Taken further, the amount of pancreatic necrosis directly relates to theoutcomes of mortality and length of stay [3,4]. The amount of necrosis deter-mines the CT severity index. We have relied heavily on the CT severity indexto categorize patients for clinical studies [4].

Caution must be exercised, because there is no substitute for clinical evalu-ation. All decisions are made on clinical findings, not imaging studies or the CTseverity index. If pancreatic ductal disruption is present, it will evolve into oneor more of six potential outcomes on subsequent imaging studies. The out-comes depend on the severity of the ductal disruption and the extent of necro-sis. These six outcomes are as follows:

1. Resolution, because many of these ductal leaks seal.2. Peripancreatic fluid collection(s) with or without contained pancreatic en-

zymes. The latter indicates a persistent pancreatic duct leak.3. Over time, a fluid collection develops a wall secondary to chronic inflamma-

tion and forms a pseudocyst that may evolve into an infected pseudocyst.4. Infected pseudocyst, a kind of pancreatic abscess that occurs late in the clin-

ical course, usually after 30 days.5. Sterile necrosis.6. Infected necrosis, with or without a pancreatic abscess.

Fig. 1. The multidisciplinary team at our hospital that operates from the common algorithm out-lined in this chapter. The members include individuals from interventional radiology, therapeuticendoscopy, and general surgery. These specialties are always available to apply the appropri-ate treatment, which is based on experience and clinical judgment, not diagnostic tests.

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These terms must be defined, but with a mechanism to explain the mysteryof pancreatitis.

Pancreatic necrosisPancreatic necrosis is devitalized tissue that can be either pancreatic paren-chyma or peripancreatic tissue. In our experience, most of the necrosum is peri-pancreatic. Sakorafas and colleagues [5] found that some cases could be totallyextrapancreatic. If a segment of the gland is necrotic then the location is usuallythe central area of the gland (pancreatic body) because of the anastomosing vas-cular network or watershed blood supply in this location. Successful percutane-ous drainage of a peripancreatic fluid collection in the lesser sac or pancreaticdebridement in this area frequently is associated with the body of the pancreasbeing missing on subsequent CT scans, which is termed the ‘‘disconnectedgland syndrome.’’ This syndrome is a commonly observed pattern during re-solving parenchymal necrosis. This syndrome is most often associated witha persistent pancreatic fistula. Enzyme-rich drainage is caused by an end-pan-creatic fistula from the separated upstream pancreatic remnant.

Peripancreatic fluid collections, pseudocyst, and pancreatic abscessTo re-emphasize the role of ductal disruption and determine how peripancre-atic necrosis may occur, one must understand the mechanism of ductal disrup-tion. For many reasons one of the small side branches of the pancreatic ductalsystem begins to leak, which results in a pancreatic fistula. If contained withinthe pancreatic capsule, the fistula is self-limited and self-healing. The leak mayoccur from focal necrosis (alcohol etiology) or downstream ductal obstructionwith side branch blow-out (passage of a gallstone, too much pressure duringERCP). For whatever reason, if the rupture breaks through the capsule, theperipancreatic enzyme-rich fluid bathes peripancreatic tissues, depending onwhere the ductal disruption is located. In more than two thirds of our casesthe disruption is to the left of the portal vein and a peripancreatic fluid collec-tion occurs in the lesser sac. If the source of fluid declines as the ductal disrup-tion seals then the fluid is reabsorbed or walled off to form a pseudocyst. If thisfluid is infected or becomes infected, the result is a pancreatic abscess, whichusually occurs 3 to 4 weeks after the initial clinical presentation. We rarelysee a pancreatic abscess (pus in an infected peripancreatic fluid collection orpseudocyst) because with new technology, at least in our institution, all of thesesymptomatic peripancreatic fluid collections are percutaneously drained.A pseudocyst is uncommonly seen for the same reason–unless a patient istransferred with untreated disease.

CAVEATS FOR IMAGING AND USING THESE DEFINITIONSBecause pancreatic necrosis is devitalized tissue found at surgery, one must re-member that ‘‘pancreatic necrosis’’ mentioned in a CT scan report usually rep-resents nonenhancement of the pancreatic tissue. This is simply a relativedecrease in blood flow compared to other solid organs or other parts of the

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pancreas and not necessarily true pancreatic necrosis. The interchangeable useof ‘‘nonenhancement’’ seen on imaging with pancreatic necrosis can lead tomisunderstanding of the disease process and unnecessary procedures.

One of the best ways to improve surgical judgment with pancreatic necrosisis not to rely solely on radiologic reports. Rather the CT scan should be re-viewed personally with the radiologist. Over the years of doing this we haveobserved the following patterns. When present, the peripancreatic fluid collec-tions make visualizing the pancreatic parenchyma impossible, and these casesare often termed ‘‘necrosis.’’ Support for this concept resides in subsequentCT scans. After the fluid has been drained or reabsorbed the previouslyseen parenchymal nonenhancement is absent. Patients should be assumed tohave necrosis if peripancreatic fluid collections are not interfering with paren-chymal visualization during a contrast-enhanced CT scan and if the paren-chyma shows nonenhancement.

TREATMENT GOAL IS SINGLE-DIGIT MORTALITY THROUGHDECREASED NEED OF NECROSECTOMYThe term ‘‘necrosis’’ unfortunately instills the knee-jerk response to perform ne-crosectomy. Over time the necrosis dissolves (necrolyses) or becomes infected orboth. Infected pancreatic necrosis is an indication for operative debridement inmost medical centers throughout the world. In our institution, however, we be-gin with clinical observations to make decisions. Our first treatment maneuver ispercutaneous drainage followed by CT scans every third day. At that time tubemanipulation or exchanges with upsizing might be necessary based on patencyand location of tubes during sinography. The patient is carefully monitored forclinical progress. This algorithm has lowered drastically the need for pancreaticnecrosectomy in our institution while keeping the mortality rate in single digits.In the most severe subset of 73 patients with necrosis we observed that our ne-crosectomy rate fell to 21%, whereas the mortality rate was 11% [4].

The presence of a persistent ductal disruption increases the likelihood for pan-creatic necrosectomy [3]. The definition of ductal disruption used in that studywas an enzyme-rich fluid coming from a percutaneous drain or a disruption dem-onstrated by ERCP. Ductal disruption is an important item to seek because con-trolling the leak at its source prevents uncontrolled spread of enzyme-rich juice,digestive necrosis, and ultimately infection in this dead space. Draining the leakat the source of ductal disruption and minimizing the resulting peripancreatic ne-crosis may be all that is necessary to allow the process to improve.

One caveat here: when ERCP is used, it colonizes a sterile fluid collectionwith gut-derived bacteria. To prevent abscess formation in a sterile fluid collec-tion any ductal disruption observed by ERCP connecting to that fluid collec-tion must be drained within 24 hours. Infecting a sterile environment duringERCP and then not draining the collection can lead to severe septic complica-tions. ERCP has developed an unfortunate reputation that has led to others notusing this valuable technique. Because the presence and location of the disrup-tion are so important for truncating the disease, it is also important to not

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provide an iatrogenic abscess. Before percutaneous drainage is attempted weuse endoscopically placed main pancreatic duct stents through the papilla to de-compress the potentially infected area. If this fails then a percutaneous drain isrequired. This discussion emphasizes the importance of a multidisciplinaryteam in order to use this algorithm (ie, a hospital team of interventional radi-ologists, therapeutic endoscopists, and surgeons using a coordinated approachwith the principles of surgical drainage).

Pancreatic necrosectomy is the last option in symptomatic patients with pan-creatic necrosis. Depending on the expertise and preference of the managingteam the options for treatment include

� Percutaneous drainage with large bore catheters that are frequently manipu-lated and changed under fluoroscopic control every 3 days regardless of clin-ical condition. These tube exchanges are preceded with a CT scan.

� Trans-drain tract endoscopic debridement that admits a 10-mm working lapa-roscope. The latter have been hampered by limited ability to remove ne-crosum, which requires multiple procedures.

� Open pancreatic necrosectomy.

PERCUTANEOUS CATHETER NECROSECTOMY: REVIEWOF RECENT LITERATUREAlthough multiple articles have been published about the treatment of acutepancreatitis by percutaneous drainage, only a handful of articles specifically ad-dress pancreatic necrosis (Table 1).

One of the first articles regarding percutaneous treatment of pancreatic ne-crosis was by Freeny and colleagues [2]. In their series, 34 patients with acute

Table 1Percutaneous drainage

SeriesPatients(n)

Infected(%)

Mortality(%)

Success(%) Morbidity

Freeny, 1998 34 100 4 (12) 16 (47) Enteric fistula 8 (24%)Pancreatic

fistula9 (26%)

Sepsis 9 (26%)Hemorrhage 1 (3%)

Echenique, 1998 20 100 0 20 (100) Enteric fistula 3 (15%)Pancreatic

fistula7 (35%)

Diabetes 5 (25%)Renal failure 2 (10%)

Gouzi, 1999 32 81 5 (15) 21 (65) Fistula 17 (53%)Szentkereszty,

200224 NS 3 (12.5) 3 (12.5) None

Total 110 12 (11) 60 (54) 61 (55%)

Abbreviation: NS, not stated.Adapted from Refs. [2,6–8].

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necrotizing pancreatitis were treated primarily by percutaneous catheter drain-age. Of these patients, 16 (47%) were cured by percutaneous drainage alone.Sepsis was controlled in an additional 9 patients. The important factors pre-sented in this paper include use of large bore catheters (up to 28 Fr), frequentcatheter checks under fluoroscopy using contrast medium, frequent change ofcatheters (146 times, average 4 per patient), and vigorous intermittent manualirrigation with normal saline.

Echenique and colleagues [6] presented their experience with 20 patientswith infected pancreatic necrosis treated by percutaneous drainage alone. Intheir series the method used was different from that of Freeny because the cath-eters were smaller bore (10–14 Fr) and patients underwent ‘‘debridement ses-sions’’ under fluoroscopic guidance. These ‘‘debridement sessions’’ includedusing irrigations with heparinized saline diluted with contrast material, use ofsuction debridement via vascular sheaths, and mechanical debridement usingstone retrieval baskets. This technique was successful in all of their patients.

Since then, other papers have been presented with slight modifications intheir methods without significant difference in outcomes. In these papers, suc-cess has been defined as patients surviving necrotizing pancreatitis with percu-taneous means alone (ie, avoiding open surgery (Table 1) [2,6–8].

The low number of articles addressing percutaneous drainage for pancreaticnecrosis can be because of multiple factors, including lack of adherence to strictdefinitions of complications of acute pancreatitis (eg, pancreatic abscess, pseu-docysts and necrosis), lack of vigilance and collaboration between multiple dis-ciplines within different institutions; and lack of patience with percutaneousapproach for treatment of pancreatic and peripancreatic necrosis.

We believe that percutaneous drainage for treatment of infected pancreatic ne-crosis is an indispensable tool to temporize sepsis, especially in the acute phase ofdisease presentation. To take on this approach requires vigilance and commit-ment to catheter care, patient management, and using a multidisciplinary ap-proach. On many occasions we have noted patients who have been transferredto our institution for refractory pancreatitis in which percutaneous drainagehas been considered a failure. In most cases this is caused by lack of attentionto catheter care. Presence of necrotic debris often causes catheter occlusion. Itis imperative to exchange and upsize catheters frequently (every 3 days) to ensuretheir patency. Frequent CT scans (every 3 days) also help identify loculatedundrained collections or lobulations of already drained collections. These imagesare then used to manipulate catheters into the undrained lobulations or place newcatheters in undrained collections. In our experience using these methods, it ispossible to avoid surgical intervention in most patients with acute necrotizingpancreatitis and decrease the mortality rate of this disease.

PERCUTANEOUS ENDOSCOPIC NECROSECTOMY: REVIEWOF RECENT LITERATURECarter and colleagues [9] described the development of a minimally invasiveapproach to pancreatic necrosectomy, which included placement of an initial

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8 Fr catheter in the infected cavity, usually from the left flank, using CT guid-ance. Patients were then transferred to the operating room where under generalanesthesia the tract was dilated to 30 Fr. Subsequently, a nephroscope was usedin combination with grasping forceps to perform piecemeal removal of solid de-bris. A 28 Fr catheter in combination with an 8 Fr catheter were left in the cav-ity for continuous lavage. Using this method, eight of ten patients were curedwithout requiring open surgery.

Since Carter’s publication, other reports of this method have followed withslight modifications (Table 2) [9–12]. Although the success rate of this tech-nique seems to be better than the percutaneous drainage approach, it requiresgeneral anesthesia, time, and expertise of the operator for success. Because ofa low number of total patients presented in these reports, it is too early to assessthe true success rate and morbidity of this procedure compared to the manyreports regarding open necrosectomy. Future studies may shed more light

Table 2Percutaneous endoscopic necrosectomy9–12

SeriesPatients(n)

Infected(%)

Mortality(%)

Success(%)a Morbidity

Carter, 2000 10 100 2 (20) 8 (80) Multiorgan failure 1 (10%)Hemorrhage 1 (10%)Gastric ileus 1 (10%)Late pseudocyst 2 (20%)

Connor, 2003 24 100 6 (25) 18 (75) Multiorgan failure 11 (46%)Hemorrhage 3 (13%)Enteric fistula 2 (8%)Thromboembolic 2 (8%)Splenic V thrombosis 1 (4%)Myocardial

infarction1 (4%)

Sepsis 2 (8%)Persistent pancreatic

fistula4 (17%)

Biliary stricture 2 (8%)Late pseudocyst 1 (4%)

Risse, 2004 6 100 0 5 (83) Late pseudocyst 1 (17%)Postprocedural

peritonitis1 (17%)

Diabetes mellitus 1 (17%)Cheung, 2005 8 100 1 (12.5) 5 (62.5) Intestinal fistula 4 (50%)

Gastric ileus 1 (13%)Persistent sepsis 3 (38%)

Total 48 9 (18.8) 36 (75) 45b

aSuccess is defined as number of patients surviving necrotizing pancreatitis with percutaneous meansalone (ie, not requiring open surgical intervention).

bTotal complications in 48 patients. Percentages are not used because the total number under morbidityreflects the number of complications and not the number of patients.

Adapted from Refs. [9–12].

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on the feasibility of the endoscopic percutaneous approach in treatment of pan-creatic necrosis.

THE MODERN OPEN PANCREATIC NECROSECTOMY WITHPOSTOPERATIVE RADIOLOGIC ASSISTANCE: TECHNIQUEThe modern open necrosectomy should be viewed as radiologically assisted inthe postoperative period.

IncisionUse an upper midline incision above the umbilicus to minimize the risk of inci-sional hernia, a frequently reported complication. This approach preserves therectus abdominus muscles and allows great exposure to the areas of interest.Because percutaneous drains are rarely placed through the midline, the midlineincision avoids the location of percutaneous drains. These drain tracts shouldbe preserved because they are used repetitively for subsequent tube changes.Preserve the radiologically placed drains over each pararenal space. This path-way usually represents a great angle of percutaneous access to the lesser sac.When the fascia is closed, use interrupted wide figure-8 nonabsorbable mono-filament sutures for this contaminated wound. The skin is left open and al-lowed to close by secondary intention.

Omental preservationExperimental evidence shows that the omentum prevents mortality and infec-tion with pancreatic duct disruption [13]. The omentum is widely mobilized offthe entire transverse colon through the avascular plane between the omentumand the transverse colon. Besides preserving the omentum, this maneuver pre-serves the transverse mesocolon. The latter remains a barrier and protects theinferior abdominal contents from contamination postoperatively. We do notrecommend debridement through the mesocolon.

Keep instruments simpleUse just two instruments—the finger and a ring forceps—to avoid bleeding. Fin-ger dissection begins at the top of the necrosum and breaks it up with a rollingmotion. A ring forceps can be used to help peel the densely adherent ‘‘peanutbutter’’ gently off surrounding organs and major vessels. Prior surgical experi-ence dissecting in this area under elective conditions is a huge help to avoiddamage of adjacent organs and major vessels. Follow the planes that alreadyhave been outlined by the necrosum. Any normal pancreas encounteredshould not be debrided. This warning is supported by the observation of a nor-mal ERCP months after the surgeon ‘‘removed’’ the entire pancreas during ne-crosectomy. This observation also supports the concept that most ‘‘necrosis’’during necrosectomy may be just peripancreatic tissue.

Use the CT scan as a mapThe necrosum at this stage is ‘‘mature.’’ By this time in the disease course, afterall of the other previously tried minimally invasive techniques have failed, theextending peripancreatic necrosis has been truncated by decompressing the

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ductal disruption. This approach allows the surrounding tissue to wall off thenecrosis. The static necrosum is fairly easy to remove with the dissecting fingerand a ring forceps. We suggest that the necrosum be weighed. At least 25 g isusually removed. Weights in excess of 50 g may connote a significant mortalityrate. Note that arresting the dynamic spreading necrosis with ductal decom-pression or percutaneous drains directed at the site of leak may truncate theamount of necrosis.

Percutaneous drains need to be maintainedThese large bore (24–28 Fr) closed-suction catheters must be replaced contin-ually. Occasionally a new drain site must be used to gain better access. Duringthe time of open necrosectomy we use drains obtained from the interventionalradiology department, which ensures ease of exchange over guidewires. Usu-ally just two catheters are required, and they cross from both sides of the ab-domen (Fig. 2). We cannot overemphasize that it is mandatory to exchangethese catheters repetitively in the interventional radiology department in thepostoperative period. Just as in the preoperative period, these catheters mustbe maintained in the postoperative period (including the period after dischargefrom the hospital). Begin by exchanging the catheters at 3 days after surgeryand then perform sinogram tube checks every 3 days with CT scans to

Fig. 2. The final position of large bore drainage catheters after necrosectomy is depicted.Ideally these catheters should meet in the midline. The picture shows the right catheter enteringa surgeon-placed drain in the right subcostal area that goes under the duodenum to lie underthe superior mesenteric vein. The left catheter penetrated the dorsal flank and was originallyplaced by interventional radiology only to be exchanged at the time of necrosectomy fora larger catheter (28 Fr). The latter catheter pathway is best acquired by interventional tech-nique as it courses over the left kidney and under the splenic flexure and spleen to enter thelesser sac. This dorsal flank entrance site is better tolerated by the patient than a subcostalsite. (From Traverso LW. Pancreatic necrosectomy: definitions and technique. How I do it.J Gastrointest Surg 2005;9:436–9; with permission from the Society for Surgery of the Alimen-tary Tract.)

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determine if the cavities are closing and the tubes are open. Soon the frequencycan be decreased to weekly. After several weeks the tubes can be downsized asthe cavity decreases in size. The modern open necrosectomy should be viewedas radiologically assisted in the postoperative period.

Concomitant cholecystectomySmoldering cholecystitis can be overlooked easily in sick patients because per-sistent sepsis is attributed to the necrosis. The gallbladder should be removed,because it can be the cause of recurrent gallstone pancreatitis or smolderingcholecystitis from cystic duct occlusion. Obtain an intraoperative cholangio-gram, because 31% of patients have reflux into the main pancreatic duct andthe cholangiogram provides valuable ‘‘plumbing’’ information within themain pancreatic duct.

SUMMARYAlthough we recommend the team approach for the treatment of pancreatic ne-crosis, we cannot support our method with evidence-based medicine. The fewreports available (presented in this article) suggest an improvement by avoidingsurgery in many cases and with a low mortality. Two important prerequisitesare necessary to begin this team method. First is the assembly of a team, whichrequires years of recruitment using influence and leadership at centers of exper-tise in the treatment of pancreatic necrosis. Second, and possibly just as difficultas team assembly, is the design and use of a common algorithm that allows thereporting of data supported with the ‘‘power of n.’’

References[1] Bradley EL III. A clinically based classification system for acute pancreatitis: summary of the

International Symposium on Acute Pancreatitis. Atlanta, GA, September 11 through 13,1992. Arch Surg 1993;128:586–90.

[2] Freeny PC, Hauptmann E, Althaus SJ, et al. Percutaneous CT-guided catheter drainage ofinfected acute necrotizing pancreatitis: techniques and results. AJR Am J Roentgenol1998;170:969–75.

[3] Lau ST, Simchuk EJ, Kozarek RA, et al. A pancreatic ductal leak should be sought to directtreatment in patients with acute pancreatitis. Am J Surg 2001;181:411–5.

[4] Simchuk EJ, Traverso LW, Nukui Y, et al. Computed tomography severity index is a predictorof outcomes for severe pancreatitis. Am J Surg 2000;179:352–5.

[5] Sakorafas GH, Tsiotos GG, Sarr MG. Extrapancreatic necrotizing pancreatitis with viablepancreas: a previously under-appreciated entity. J Am Coll Surg 1999;188:643–8.

[6] Echenique AM, Sleeman D, Yrizarry J, et al. Percutaneous catheter-directed debridement ofinfected pancreatic necrosis: results in 20 patients. J Vasc Interv Radiol 1998;9:565–71.

[7] Gouzi JL, Bloom E, Julio C, et al. Percutaneous drainage of infected pancreatic necrosis: analternative to surgery. Chirurgie 1999;124:31–7.

[8] Szentkereszty Z, Kerekes L, Hallay J, et al. CT-guided percutaneous drainage in the treat-ment of acute necrotizing pancreatitis. Magy Seb 2001;54:11–4.

[9] Carter CR, McKay CJ, Imrie CW. Percutaneous necrosectomy and sinus tract endoscopy inthe management of infected pancreatic necrosis: an initial experience. Ann Surg2000;232:175–80.

[10] Connor S, Ghaneh P, Raraty M, et al. Minimally invasive retroperitoneal pancreatic ne-crosectomy. Dig Surg 2003;20:270–7.

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[11] Risse O, Auguste T, Delannoy P, et al. Percutaneous video-assisted necrosectomy for infectedpancreatic necrosis. Gastroenterol Clin Biol 2004;28:868–71.

[12] Cheung MT, Ho CN, Siu KW, et al. Percutaneous drainage and necrosectomy in the man-agement of pancreatic necrosis. Aust N Z J Surg 2005;75:204–7.

[13] Traverso LW, MacFarlane SK. Pancreatic juice in the peritoneal cavity: antibiotics or omen-tal preservation prevent mortality. J Surg Res 1987;43:220–5.